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Owenpharm Block 3 > Antibacterials > Flashcards

Antibacterials Flashcards

1
Q

What is the mechanism for Tetracyclines?

Transport into cell
Mechanism
-cidal or -static?

A
  1. Transported into cells by protein-carrier system
  2. Prevent attachment of aminoacyl-tRNA bind to 30s ribosomal subunits.
  3. Is bacteriostatic
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2
Q

What is the most common method for Tetracycline resistance?

A
  1. Drug efflux pump - cross resistance common
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3
Q

What are tetracyclines “preferred” agents for?

A

“Unusual” bugs:

Rickettsia
Lyme disease (Borrelia)
Chlamydia, Mycoplasma, Ureaplasma
Chancroid (Haemophilus ducreyi)

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4
Q

What are two examples of Tetracyclines?

A
  1. Doxycycline
  2. Minocycline
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5
Q
  1. When would Doxycycline be used instead of Minocycline?
  2. When and why would Minocycline be prefered?
  3. What diseases is doxy and mino both an alternative treatment for?
  4. What is an important chemical aspect of tetracyclines?
A
  1. For patients with impaired renal function
  2. For prophylaxis of N. meningitidis because it is most lipophilic
  3. PenG-sensitive syphilis and uncomplicated gonorrhea
  4. Calcium binding: minocycline > doxycycline
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6
Q
  1. What route/routes is tetracycline available for administration?
  2. What additional instructions should be given with oral route?
A
  1. Oral and Parenteral
  2. Don’t take with calcium containing foods, antacids etc: due to calcium binding reducing efficacy/potency.
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7
Q

What are the most significant side effects for tetracyclines other than nausea/vomitting?

A
  1. Enterocolitis
  2. Candida superinfection in colon
  3. Photosensitization with rash
  4. Teeth discoloration: avoid in children & pregnancy
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8
Q
  1. What new drug class is Tigecycline (2006) part?
  2. What is the mechanism for Tigecycline?
  3. What is the benefit regarding resistance?
A
  1. Glycylcyclines: a glycylamido modification of minocycline
  2. Same as Tetracyclines (30s binding) but also binds to additional unique site in the ribosome
  3. No cross-resistance with other antibacterials including tetracyclines
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9
Q
  1. What are the primary uses for Tigecycline?
  2. What is its bacteriostatic profile?
A
  1. Skin/skin structure infections
    complicated intra-abdominal
    community-acquired pneumonia.
  2. G-: E.coli, Citrobacter, Klebsiella, Enterobacter
    * *G+:** Staph (MSSA & MRSA), Strep
    * *Anaerobes:** Bacteroides, C. perfringens
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10
Q
  1. What is the primary side effect of Tigecycline?
  2. What was the FDA alert released in 2010?
A
  1. Enterocolitis, also calcium binding
  2. Increased risk of death: use as last resort.
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11
Q

What is the mechanism of Chloramphenicol?

A

Interferes with aminoacyl-tRNA binding to 50s** ribosome** and inhibits peptide bond formation. It is bacteriostatic.

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12
Q
  1. What is the bacteriostatic profile of Chloramphenicol?
  2. What limits its use?
A
  1. Broad spectrum: aerobes and anaerobes, G+ & G-
  2. Severity of side effects.
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13
Q

What are the two most common current indications for Chloramphenicol?

A
  1. Meningitis: alternative for cephalosporin allergy
  2. Brain abcesses
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14
Q

What are the major side effects for Chloramphenicol?

A
  1. Bone marrow depression: Fatal aplastic anemia (1 : 30,000)
  2. Grey baby syndrome
  3. Optic neuritis and blindness
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15
Q

What are the primary examples of Macrolides for this course?

A
  1. Erythromycin
  2. Clarithromycin
  3. Azithromycin
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16
Q

What is the mechanism for the bacteriostatic action of Macrolides?

A

Binds to 50s subunit, blocks translocation along ribosomes

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17
Q

What is the static profile for Erythromycin?

A
  1. G+: Strep. infections in penicillin allergy, Staph.
  2. “Unusual” bugs: Chlamydia, Mycoplasma, Legionella, Bordetella
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18
Q

What are the primary side effects for Erythromycin?

A
  1. Nausea, vomiting: enhanced GI motility
  2. Inhibition of CYP3A metabolism
  3. Increased risk of arrythmia and cardiac arrest
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19
Q

Why would Clarithromycin be preferred over Erythromycin?

A
  1. Better kinetics: less frequent dosing
  2. Less GI motility effects (~50% less)
  3. Somewhat wider antibacterial spectrum
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20
Q

What are the primary indications for Clarithromycin?

A
  1. Haemophilus influenzae, Moraxella
  2. Pen. resistant Strep. pneumoniae
  3. Atypical mycobacteria
  4. Helicobacter pylori (clarithro + amoxicillin + acid blocker)
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21
Q
  1. What is Azythromycin most frequently used for?
A
  1. Outpatient respiratory tract infections: Pneumonia
  2. Genital infections: Chlamydia
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22
Q
  1. What is unique about Azithromycin that increases its utility?
  2. What is the order of severity of side effects among the macrolides?
  3. What cardiac effect can Erythromycin and Azithromycin have?
A
  1. High tissue levels even after cessation of drug: 3 day elimination
  2. Erythromycin > Clarithromycin > Azithromycin
  3. QT prolongation
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23
Q
  1. What is the mechanism for Clindamycin?
  2. What is its significant side effect?
A
  1. Binds to 50s ribosomal subunit, blocks translocation along ribosomes
  2. Enterocolitis : C. diff
    Hepatotoxicit
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24
Q

What is the bacteriostatic profile for Clindamycin?

A
  1. G+ cocci: Strep. and MSSA, flesh-eating streptococci, not for enterococcus
  2. Anaerobes: including Bacteroides fragilis, not for C.Diff
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25
Q
  1. What is the class for Linezolid?
  2. What is its mechanism?
  3. What is the bacterio__static profile for Linezolid?
A
  1. Oxazilidinone
  2. Inhibits protein synthesis
    Binds 50s ribosome subunit, interfering with formation of 70s initiation complex
  3. Staph. and Enterococcus
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26
Q

What are the approved uses for Linezolid?

A
  1. VRE
  2. Staph. aureus (MRSA, MSSA)
  3. Strep. grp A and B
  4. Strep. pneumoniae
  5. Staph. pneumonia
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27
Q

What are the side effects for Linezolid?

A
  1. Non-selective inhibitor of MAO
  2. Diarrhea, superinfection including enterocolitis
  3. Headache, Nausea/vomiting
  4. Bone marrow suppression
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28
Q

What are the two examples of anti-folate drugs that inhibit folate synthesis?

A
  1. Sulfamethoxazole, Sulfadiazine
  2. Trimethoprim
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29
Q

What is the bacteriostatic mechanism for Sulfonamides?

A

Competitive analogue of p-aminobenzoic acid, a precursor in folate synthesis

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30
Q
  1. What is the primary use for sulfamethoxazole?
  2. What is the primary use for silver sulfadiazine?
A
  1. Used in combination with Trimethoprim for empiric treatment of cystitis
  2. Used topically for burn infection prevention
31
Q

What are the non-GI side effects of Sulfonamides?

A
  1. Renal damage (crystalluria)
  2. Inhibits CYP2C9 metabolism (Warfarin reaction)
32
Q

What is the mechanism for Trimethoprim?

A

Inhibition of folate synthesis through competitive inhibition of dihydrofolate reductase

33
Q
  1. What is the unique benefit of combining Trimethoprim and Sulfamethoxazole?
  2. What are the primary uses for TMP/SMX?
  3. What major side effect is added with Trimethoprim is added to Sulfamethoxazole?
A
  1. Two static agents become bactericidal.
  2. Uncomplicated UTIs
    Upper respiratory tract and ear
    GI infections: salmonella, shigella
    Pneumocystis jiroveci
  3. Rash, Bone marrow suppression
34
Q
  1. What is the first choice for uncomplicated cystitis in non-pregnant women?
  2. What are the secondary choices?
A
  1. TMP/SMX (Should limit Cipro due to resistance)
  2. Nitrofurantoin or Fosfomycin
35
Q

What are the most significant reasons for Antibacterial failure?

A
  1. Drug choice: susceptibility
    penetration, resistance, superinfection
  2. Host factors: abscess? host immune respone? foreign body?
36
Q

What are the top four drugs for HA-MRSA?

A
  1. Vancomycin
  2. Linezolid
  3. Daptomycin
  4. Tigecycline
37
Q

What are the top four drugs for CA-MRSA?

A
  1. Linezolid
  2. Doxycycline, Minocycline
  3. Clindamycin
  4. TMP-SMX
38
Q

What infections should bactericidal drugs have an advantage?

A
  1. Patients with compromised immune system
  2. In the following sites in normal patients:
    meningitis
    endocarditis
    deep bone infections
    artificial device implants
39
Q
  1. What does time-dependent killing mean?
  2. What does concentration dependent killing mean?
  3. When do B-lactams work best?
  4. What class of antibacterials exhibit concentration dependent killing?
  5. What drug class is dependent on concentration x time (area under the curve) (AUC24/MIC)?
A
  1. Amount (%) of time above the MIC create effect.
  2. Peak concentration (Cmax) creates effect
  3. When they exceed 4x the MIC for >50% of total time
  4. Aminoglycosides
  5. Quinolones
40
Q
  1. Are B-lactams -cidal or -static?
  2. When is B-lactam activity maximal?
A
  1. -cidal due to destruction of the cell wall
  2. On actively growing bacteria.
41
Q
  1. What is the mechanism for B-lactam antibiotics?
  2. What does this do?
  3. Why do some patients get chills/fever/aching after administration of a B-lactam?
A
  1. Competitive, irreversible, covalent binding to PBPs
  2. Inhibits the transpeptidase activity that catalyzes cell wall cross-links.
  3. Rapid bacterial lysis can cause symptoms
42
Q

What are the three mechanisms for B-lactam resistance?

A
  1. Beta-lactamase
  2. Altered PBPs
  3. Beta-lactam can’t reach PBPs
43
Q

What secondary ability does B-lactamase have that can cause problems?

A

It can protect B-lactamase negative bacteria in the vicinity.

44
Q

Are there only a few B-lactamases or many?

A

There are many. Over 400 have been reported.

45
Q
  1. B-lactams are time-dependent killers. What does this mean for successful treatment?
  2. What is the relative length of dosing interval for B-lactams and why?
A
  1. The drug must be 4-fold above the MIC for >50% of total treatment time.
  2. Shorter dosing intervals because of short t1/2
46
Q
  1. Penicillins typically have what relative penetration into the CSF? When might this change?
  2. How are penicillins eliminated? What causes decreased elimination?
  3. What is the relative half-life of penicilins?
A
  1. Low penetration into CSF. Increases during meningitis.
  2. Renal. Anionic drugs (probenecid) compete for the same anion transports.
  3. Short half lives
47
Q
  1. What is the difference between PenV and PenG in terms of their **ROUTE **of admin?
  2. What types of bugs are the best against?
A
  1. PenV is oral, PenG is IM/IV
  2. Anaerobes, gram-pos.
48
Q

What is the first line antibiotic for strep throat?

A

PenV or PenG

49
Q

What kind of activity does PenG and V have against gram-neg. bacteria? What is an example of one that it treats?

A

It has limited activity. Can treat Neisseria meningitidis.

50
Q

Name a spirochete that PenG and PenV treats?

51
Q

Which has a longer period of release from IM administration?

PenG
PenG procaine
PenG benzathine

A

PenG benzathine, this is why it is preferred for syphilis

52
Q

What drug is best for B-lactamase positive staphylococci?

A

Oxacillin or other “methicillin” type drugs.

53
Q
  1. What type of coverage does Ampicillin and Amoxicillin provide?
A
  1. Reasonable gram-pos. spectrum, Expanded gram-neg. spectrum.
54
Q

What is the drug of choice for otitis media and an alternate choice for Lyme disease?

A

Amoxicillin

55
Q

What are 2 important uses for Ampicillin?

A
  1. Meningitis (Neisseria, Listeria)
  2. GI infections (less absorption of oral dose = more in GI tract)
56
Q

What are two penicillins with extended gram-negative coverage?

A

Ticarcillin and Piperacillin

57
Q
  1. What type of gram negative bacteria is Ticarcillin good for?
  2. What is a weakness of Ticarcillin?
A
    1. Pseudomonas aeruginosa*.
      1. It is susceptible to B-lactamases.
58
Q

What is Piperacillin good for in addition to P. aeruginosa like Ticarcillin?

A
  1. Klebsiella, and Ticarcillin resistant Pseudomonas.
59
Q
  1. What percentage of very severe penicillin reactions report having had penicillin previously?
  2. What is a way to predict severe allergic reaction?
A
  1. 70%
  2. Pre-pen: 90-95% reliable skin test
60
Q

What are some other uncommon but more severe side effects of penicillins?

A
  1. Elevated liver enzymes
  2. Hemolytic anemia
  3. Seizures
61
Q
  1. What are two B-lactamase inhibitors?
  2. How do they work?
  3. What are some B-lactams that have restored utility uzing a B-lactamase inhibitor?
A
  1. Clavulanic acid and Tazobactam
  2. They are B-lactam “analogs” that bind irreversibly to B-lactamase
  3. Ampicillin, Amoxicillin, Ticarcillin, Piperacillin
62
Q

What are two examples of B-lactamase inhibitor combinations?

A

Amoxicillin + Clavulanic acid
Piperacillin + Tazobactam

63
Q
  1. What is penicillin-resistant S. pneumoniae related to?
  2. What is MRSA’s mechanism for resistance?
A
  1. Altered PBPs - Gram pos. bugs don’t use B-lactamase
  2. Acquisition of new PBP2a encoded by MecA
64
Q
  1. What is the general distribution of Cephalosporins?
  2. What route of admin is for the majority of Cephalosporins?
  3. What is the mechanism of Cephalosporins?
A
  1. They are well distributed, but only some reach the CSF (3rd generation and one 2nd generation)
  2. By injection (IM/IV)
  3. Binds to PBPs to inhibit PDG synthesis (same as Penicillins)
66
Q
  1. What is the coverage profile for 1st generation Cephalosporins?
  2. What is a common use for 1st generation cephalosporins?
A
  1. Mostly gram-pos. spectrum: good alternative for Staph. & Strep.
  2. Uncomplicated outpatient skin infections, surgical prophylaxis for skin flora
67
Q
  1. What are two examples of 1st generation cephalosporins?
  2. Which drug has best gram-pos. activity of 1st generation cephalosporins?
A
  1. Cefazolin (Ancef) and Cephalexin (Keflex)
  2. Cefazolin (Ancef) - reason why it is top
68
Q
  1. What are two examples of 2nd generation cephalosporins?
  2. What is the only 2nd generation drug that can penetrate the CSF?
  3. Which is good for anaerobes including some strains of B. fragilis?
  4. Which is good for Haemophilus?
  5. What increases the efficacy of the 2nd generations?
A
  1. Cefuroxime and Cefoxitin
  2. Cefuroxime
  3. Cefoxitin
  4. Cefuroxime
  5. Good tolerance to many gram-neg B-lactamases.
69
Q

What are two examples of 3rd generation cephalosporins?

A

Ceftriaxone (Rocephin) and Ceftazidime

70
Q
  1. What is ceftriaxone (Rocephin) a good choice for?
  2. What is the half-life for ceftriaxone?
A
  1. Meningitis, Gonorrhea
  2. long t1/2 ~6-9 hours
71
Q
  1. What positive and what negative atribute makes ceftazidime a prominent 3rd gen. ceph. drug?
  2. What is its half life?
A
  1. It is most active of 3rd gens against Pseudomonas aeruginosa. It is the poorest 3rd gen. for gram-pos.
  2. Shorter t1/2 (~90min)
72
Q

What are 4 bugs that 3rd generations are effective against? What do they all have in common?

A

E. coli, Klebsiella, Enterobacter, Proteus

They are all gram-negative.

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